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Rizatriptan

A Review of its Efficacy in the Management of Migraine

Summary

Abstract

Rizatriptan is an orally active serotonin 5-HT1 receptor agonist selective for the 5-HT1b/1dsubtypes.

The efficacy of oral rizatriptan (5 or 10mg) has been demonstrated in large (n = 309 to 1746) well designed comparative trials with placebo and oral sumatriptan.

Two hours postdose, rizatriptan 5 or 10mg was more effective than placebo at producing pain relief or a pain free status, relieving migraine-associated symptoms and normalising functional ability. In general, rizatriptan 10mg appeared to be more effective than rizatriptan 5mg. However, recurrence rates with rizatriptan 5 and 10mg appeared to be similar to those with placebo.

Patients were significantly more likely to achieve pain relief within 2 hours after receiving rizatriptan 5mg than sumatriptan 25mg and after rizatriptan 10mg than sumatriptan 50mg. This was also observed with rizatriptan 10mg compared with sumatriptan 100mg according to an age-adjusted and a prespecified per-protocol analysis. In general, rizatriptan was better than sumatriptan at relieving migraine-associated symptoms, particularly nausea, and in normalising functional ability depending on which doses were compared. The incidence of headache recurrence, time to onset of recurrence and the need for escape medication in nonresponders appeared to be similar between rizatriptan and sumatriptan.

Over the 24 hours after the dose, rizatriptan 10mg improved the quality of life of patients with migraine compared with placebo. Rizatriptan 10mg also significantly improved work function compared with placebo and with sumatriptan 50mg.

Rizatriptan appears to be well tolerated with most adverse events being mild and transient. The most commonly experienced events included general digestive complaints, general neurological complaints, dizziness, somnolence, asthenia/ fatigue and pain and pressure sensations. In clinical trials, the overall incidence of adverse events with rizatriptan 5 or 10mg was similar to that with sumatriptan 25 or 50mg but lower than that with sumatriptan lOOmg. Chest pain was reported by 1 to 3% of rizatriptan recipients and by 3 to 6% of patients receiving sumatriptan (25, 50 or lOOmg); clinically significant effects on ECG parameters, heart rate or blood pressure were not observed with rizatriptan.

Conclusions: Rizatriptan produces pain relief and a pain free status, relieves associated symptoms of migraine, normalises functional ability and improves patient quality of life. Rizatriptan 10mg appears to be more effective than rizatriptan 5mg. In comparison with oral sumatriptan, rizatriptan may provide better relief from pain and nausea, with some evidence of a faster onset of action. Thus, rizatriptan 5 or 10mg is likely to establish a place as an effective and well tolerated agent for the management of acute migraine.

Pharmacodynamic Properties

Rizatriptan is an orally active serotonin 5-HT1 receptor agonist which selectively acts at the 5-HT1b/1d subtypes.

In vitro, at supra-therapeutic doses, rizatriptan produced greater maximum contraction of human cranial arteries and less vasoconstriction of human coronary arteries than sumatriptan.

Rizatriptan inhibited electrically-induced, but not neuropeptide-induced, vasodilation of the durai blood vessels in rats, possibly by reducing neuropeptide release. Durai plasma protein extravasation was also inhibited by rizatriptan and this action may contribute to the drug’s antimigraine effect. Rizatriptan inhibited electrically-induced firing of neurons from the trigeminal nucleus caudalis in rats, suggesting a central antinociceptive effect.

In small studies in healthy volunteers or patients with controlled hypertension, rizatriptan (0.5 to 80mg as a single dose or 10mg every 2 hours for 3 doses per day for 4 days) generally produced only small, transient increases in blood pressure and did not alter heart rate, or affect the increases in blood pressure and heart rate in response to sympathetic stimulation. However, it is important to note that, as with other 5-HT1b/1d agonists, rizatriptan is contraindicated in patients with coronary artery disease or uncontrolled hypertension.

In a small study in healthy volunteers, no additive effects on systolic blood pressure were observed when rizatriptan 10mg was added to intravenous ergot-amine 0.25mg.

Oral rizatriptan in single doses of 20 to 60mg produced a transient increase in growth hormone levels similar to that after sumatriptan 100mg, but had no effect on prolactin levels.

Pharmacokinetic Properties

Oral Administration: After single dose oral rizatriptan 5 to 60mg in healthy male volunteers, the maximum plasma concentration (Cmax) ranged from 7.8 to 90.8 µg/L, the area under the plasma concentration-time curve (AUC) ranged from 17.4 to 394.5 µg/L · h. The mean time to achieve Cmax (tmax) was 0.7 to 2.1 hours after single dose rizatriptan 2.5 to 60mg. The median tmax of rizatriptan (5 to 60mg) was significantly lower than the tmax of oral sumatriptan 100mg (1.3 vs 2.5 hours). The elimination half-life (t½) of rizatriptan was about 2 to 2.5 hours. The main route of elimination of rizatriptan is metabolism via the monoamine oxidase A enzyme; the major indole-3-acetic acid metabolite is inactive at 5-HT1b/1d receptors but a minor N-monodesmethyl metabolite has similar activity to the parent drug.

The presence of food increased the extent and decreased the rate of rizatriptan absorption without altering t½ values. Multiple rizatriptan doses increased values for absorption (Cmax, tmaxand AUC) but not elimination (t½ and renal clearance) parameters, and there was no unexpected accumulation. Pharmacokinetic parameters (Cmax, AUC and t½) appear similar in adolescent migraineurs compared with healthy volunteers. It is unclear whether rizatriptan pharmacokinetics differ between men and women.

Intravenous Administration: In healthy volunteers, plasma clearance, volume of distribution at steady state, t½ and the mean retention time in the body were similar, and AUC increased dose-proportionally after intravenous rizatriptan 10 to 60 µg/kg or 0.5 to 2.5mg (estimated as 6.5 to 42 µg/kg). However, when the rizatriptan dose was increased from 60 to 90 µg/kg or from 2.5 to 5mg (from about 33 to 42µg/kg to about 65 to 85 µg/kg), plasma clearance and volume of distribution at steady state decreased. The increase in AUC was disproportional when the rizatriptan dose was increased from 60 to 90 µg/kg.

Therapeutic Efficacy

The efficacy of oral rizatriptan (5 or 10mg) [standard tablets and orally disintegrating tablets] has been demonstrated in large (n = 309 to 1746) well designed comparative trials with placebo and oral sumatriptan.

Rizatriptan 5 or 10mg (standard tablets) was more effective than placebo at producing pain relief or a pain free status. Pain relief at 2 hours after treatment of a single migraine attack was reported in about 59 to 77% of rizatriptan recipients compared with 26 to 40% of patients receiving placebo. Furthermore, 25 to 44% of rizatriptan recipients were pain free compared with 7 to 10% of placebo recipients. The significant effect on pain relief versus placebo was generally apparent from 1 hour after the dose, although in the largest trial rizatriptan (5 and 10mg) was more effective than placebo at 30 minutes after the dose. This increased effect compared with placebo was also observed at 30 minutes after a 10mg dose in the 1 trial using the orally disintegrating tablets. A similar trend in the incidence of these 2 pain parameters was observed between rizatriptan 10mg and placebo in subsequent migraine attacks. Rizatriptan also significantly reduced the need for rescue medication at 2 hours after the dose in nonresponders to the initial dose, improved functional disability and relieved migraine-associated symptoms compared with placebo.

The incidence of headache recurrence and the time to the onset of recurrence appeared to be similar between rizatriptan 5 and 10mg and placebo. After treatment of the first recurrence, significantly more patients reported pain relief after rizatriptan 10mg, and were pain free after rizatriptan 5 and 10mg, than after placebo.

In a trial in 105 patients with migraine associated with menses, significantly more patients receiving rizatriptan 10mg than placebo reported pain relief at 2 hours (75 vs 55%).

In a comparative trial with sumatriptan, rizatriptan 5mg recipients were significantly more likely to achieve earlier pain relief within the 2 hours after the dose (primary end-point) than patients receiving sumatriptan 25mg. Rizatriptan 10mg recipients were also significantly more likely to achieve pain relief within 2 hours than patients receiving sumatriptan 50mg, and when compared with sumatriptan 100mg recipients according to an age-adjusted analysis and a prespecified per-protocol analysis.

In patients experiencing migraine-associated symptoms at baseline, at 2 hours significantly greater relief of nausea was achieved with rizatriptan 5 and 10mg than with sumatriptan 25 and 50mg, respectively, and rizatriptan 10mg was significantly better than sumatriptan 100mg at relieving nausea, phonophobia and photophobia. At 2 hours, functional ability was normalised in significantly more patients receiving rizatriptan 10mg than in sumatriptan 100mg recipients, but no significant differences were observed between rizatriptan 5mg and sumatriptan 25 or 100mg or between rizatriptan 10mg and sumatriptan 50mg.

In general, the need for escape medication at 2 hours after the dose and the incidence of headache recurrence and time to onset of recurrence appeared to be similar between rizatriptan and sumatriptan.

When quality-of-life (QOL) parameters were assessed at 24 hours after the dose, rizatriptan 5 and 10mg significantly improved all QOL parameters in 1 trial, and improved work function in another study, compared with placebo. Rizatriptan 5 and 10mg improved patient quality of life to a similar extent to sumatriptan 25 and 50mg, respectively, except for the work domain in which rizatriptan 10mg was significantly better than sumatriptan 50mg.

In a large (n = 1746) long term (≤1 year) trial, the median number of attacks during which patients reported pain relief and were pain free was significantly greater with rizatriptan 10mg than with usual treatment (typically sumatriptan) [90 vs 70% and 50 vs 29%, respectively]. However, no significant differences were observed in these parameters between rizatriptan 5mg and usual treatment, and rizatriptan 10mg was significantly more effective than rizatriptan 5mg.

Tolerability

Rizatriptan (5 or 10mg) is generally well tolerated and adverse events are usually mild and transient. The incidence of events appears to be dose related and is similar after single and multiple doses. The overall incidence of adverse events appeared to be similar between rizatriptan (5 and 10mg) and sumatriptan (25 and 50mg) but significantly lower with both rizatriptan doses than with sumatriptan 100mg.

Most adverse events occurring more commonly with rizatriptan than with placebo were related to the gastrointestinal tract or the CNS. These included general digestive complaints, general neurological complaints, dizziness, somnolence, asthenia/fatigue and pain and pressure sensations.

In clinical trials, individual events which were reported less frequently with rizatriptan (5 or 10mg) than with sumatriptan (50 or 100mg) included asthenia/ fatigue, nausea and headache. However, dry mouth was more common after rizatriptan 5mg than after sumatriptan 50mg, and dizziness occurred more frequently after rizatriptan (5 and 10mg) than after sumatriptan 25mg. These adverse events were, however, reported by relatively small percentages of patients (<10%) receiving either agent.

Chest pain was reported by 1 to 3% of rizatriptan (5 or 10mg) recipients and by 3 to 6% of patients receiving sumatriptan (25, 50 or 100mg) according to trial data. The incidence of this event was significantly greater with rizatriptan 5mg and sumatriptan 25 and 50mg than with placebo in 1 trial, but similar with rizatriptan 5 and 10mg and sumatriptan 100mg compared with placebo in another trial. In comparison with sumatriptan 100mg, the incidence of chest pain was significantly less frequent with rizatriptan 5mg but similar to that with rizatriptan 10mg. No clinically significant changes in blood pressure, heart rate, ECG parameters or laboratory parameters were observed after any agent.

The withdrawal rate from trials because of adverse events appeared to be higher with rizatriptan 5mg than with sumatriptan 25mg, similar between rizatriptan 10mg and sumatriptan 50mg and similar between both doses of rizatriptan and sumatriptan 100mg.

In the long term trial comparing rizatriptan 5 and 10mg with usual antimigraine treatment, the overall incidence of adverse events (causality not established) was similar between rizatriptan 10mg (80%) and usual treatment (78%) and both incidences were significantly higher than that with rizatriptan 5mg (68%). However, the incidence of each individual event appeared to be similar between both doses of rizatriptan and usual treatment.

Dosage and Administration

Rizatriptan is available as a standard tablet and as an orally disintegrating tablet. The orally disintegrating tablet dissolves rapidly on the tongue and may be useful for patients with swallowing difficulties or those without access to liquids during an attack.

The recommended dose of rizatriptan, from the prescribing information available in the US, is 5 or 10mg initially which can be repeated every 2 hours if necessary for recurrence to a total of 30mg in a 24-hour period. A dose reduction is generally not necessary in elderly patients.

The use of rizatriptan in children and nursing mothers has not yet been established, and use in pregnancy is only recommended after assessing the risk-benefit ratio.

Rizatriptan is contraindicated in patients with coronary artery disease or any other significant cardiovascular disease, uncontrolled hypertension, or hemiplegic or basilar migraine. It should be used with caution in patients reporting signs or symptoms suggestive of angina, patients on dialysis or in patients with moderately impaired hepatic function.

Drugs which may interact with rizatriptan or have additive effects include propranolol, monoamine oxidase inhibitors, ergotamine or ergot-containing drugs and other 5-HT1 receptor agonists. Observation of patients is advised if rizatriptan is coadministered with selective serotonin reuptake inhibitors.

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References

  1. Saper JR. Diagnosis and symptomatic treatment of migraine. Headache 1997; 37 Suppl. 1: S1–14

    PubMed  Google Scholar 

  2. Goadsby PJ, Olesen J. Diagnosis and management of migraine. BMJ 1996 May 18; 312: 1279–83

    PubMed  Article  CAS  Google Scholar 

  3. Skaer TL. Clinical presentation and treatment of migraine. Clin Ther 1996 Mar-Apr; 18: 229–45

    PubMed  Article  CAS  Google Scholar 

  4. Goadsby PJ. Diagnosis and optimum treatment of migraine. CNS Drugs 1994 Apr; 1: 245–53

    Article  Google Scholar 

  5. Perry C, Markham A. Sumatriptan: an updated review of its use in migraine. Drugs 1998 Jun; 55(6): 889–992

    PubMed  Article  CAS  Google Scholar 

  6. Merck and Co., Inc. Maxalt and Maxalt-MLT prescribing information. West Point, USA, 1998

  7. Longmore J, Razzaque Z, Shaw D, et al. Comparison of the vasoconstrictor effects of rizatriptan and sumatriptan in human isolated cranial arteries: immunohistological demonstration of the involvement of 5-HT1B-receptors. Br J Clin Pharmacol 1998; 46: 577–82

    PubMed  Article  CAS  Google Scholar 

  8. Ferro A, Longmore J, Hill RG. A comparison of the contractile effects of 5-hydroxytryptamine, sumatriptan and MK-462 on human coronary artery in vitro. Br J Clin Pharmacol 1995 Sep; 40: 245–51

    PubMed  Article  CAS  Google Scholar 

  9. Longmore J, Boulanger CM, Desta B, et al. 5-HT 1D receptor agonists and human coronary artery reactivity in vitro: crossover comparisons of 5-HT and sumatriptan with rizatriptan and L-741, 519. Br J Clin Pharmacol 1996 Oct; 42: 431–41

    PubMed  Article  CAS  Google Scholar 

  10. MaassenVanDenBrink A, Reekers M, Bax WA, et al. Coronary side-effect potential of current and prospectice antimigraine drugs. Circulation 1998; 98: 25–30

    PubMed  Article  CAS  Google Scholar 

  11. Sciberras DG, Polvino WJ, Gertz B J, et al. Initial human experience with MK-462 (rizatriptan): a novel 5-HT1d agonist. Br J Clin Pharmacol 1997 Jan; 43: 49–54

    PubMed  Article  CAS  Google Scholar 

  12. Goadsby P, Edvinsson L. Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Ann Neurol 1990; 28: 183–7

    PubMed  Article  CAS  Google Scholar 

  13. Williamson DJ, Shepheard SL, Hill RG, et al. The novel anti-migraine agent rizatriptan inhibits neurogenic durai vasodilation and extravasation. EurJ Pharmacol 1997 Jun5;328: 61–4

    Article  CAS  Google Scholar 

  14. Cumberbatch MJ, Hill RG, Hargreaves RJ. Rizatriptan has central antinociceptive effects against durally evoked responses. Eur J Pharmacol 1997 Jun 5; 328: 37–40

    PubMed  Article  CAS  Google Scholar 

  15. Sciberras DG, Majmudar N, Bowman AJ, et al. A study of the effects of MK-462 (rizatriptan), clonidine and sumatriptan on autonomic function [abstract]. Br J Clin Pharmacol 1997 May; 43: 535P

    Article  Google Scholar 

  16. Goldberg MR, Lee Y, Ermlich S, et al. Single and multiple-dose pharmacokinetics and tolerability of rizatriptan, a novel 5-HT1D/1B agonist for migraine [abstract]. Headache 1997 May; 37: 310

    Google Scholar 

  17. Noveck RJ, Bialy GP, Bradstreet TE, et al. Effects of rizatriptan on blood pressure in hypertensive patients [abstract]. Clin Pharmacol Ther 1998; 63: 184

    Google Scholar 

  18. Seidelin K, Tfelt-Hansen P, Mendel C, et al. Peripheral haemodynamic study of MK-462, ergotamine and their combination in man. Merck and Co., Inc. (USA). (Data on file)

  19. Liu L, Cheng H, Chavez C, et al. Identification of urinary metabolites of N,N-dimethyl-2-[5-(l,2,4-triazol-l-ylmethyl)-1H-indol-3-yl] ethylamine benzoate (MK-462) in humans [abstract]. Pharm Res 1994 Oct; 11 Suppl.: S–409

    Google Scholar 

  20. Lee Y, Conroy JA, Stepanavage ME, et al. Pharmacokinetics and tolerability of oral rizatriptan in healthy male and female volunteers. Br J Clin Pharmacol 1999; 47: 373–8

    PubMed  Article  CAS  Google Scholar 

  21. Cheng H, Polvino WJ, Sciberras D, et al. Pharmacokinetics and food interaction of MK-462 in healthy males. Biopharm Drug Dispos 1996 Jan; 17: 17–24

    PubMed  Article  CAS  Google Scholar 

  22. Goldberg MR, Lowry R, Musson DG, et al. Lack of pharmacokinetic and pharmacodynamic interaction between rizatriptan and paroxetine. J Clin Pharmacol 1999; 39: 192–9

    PubMed  Article  CAS  Google Scholar 

  23. Lee Y, Ermlich SJ, Sterrett AT, et al. Pharmacokinetics and tolerability of intravenous rizatriptan in healthy females. Biopharm Drug Dispos 1998; 19: 577–81

    PubMed  Article  CAS  Google Scholar 

  24. Winner P, Sadowski C, Pate D, et al. Pharmacokinetics of rizatriptan in adolescent migraineurs. Headache 1998; 38(5): 411

    Google Scholar 

  25. Teall J, Tuchman M, Cutler N, et al. Rizatriptan (MAXALT) for the acute treatment of migraine and migraine recurrence. A placebo-controlled, outpatient study. Headache 1998 Apr; 38: 281–7

    PubMed  Article  CAS  Google Scholar 

  26. Kramer MS, Matzura-Wolfe D, Polis A, et al. A placebo-controlled crossover study of rizatriptan in the treatment of multiple migraine attacks. Neurology 1998 Sep; 51: 773–81

    PubMed  Article  CAS  Google Scholar 

  27. Gijsman H, Kramer MS, Sargent J, et al. Double-blind, placebo-controlled, dose-finding study of rizatriptan (MK-462) in the acute treatment of migraine. Cephalalgia 1997 Oct; 17: 647–51

    PubMed  Article  CAS  Google Scholar 

  28. Goldstein J, Ryan R, Jiang K, et al. Crossover comparison of rizatriptan 5 mg and 10 mg versus sumatriptan 25 mg and 50 mg in migraine. Headache 1998; 38: 737–47

    PubMed  Article  CAS  Google Scholar 

  29. Tfelt-Hansen P, Teall J, Rodriguez F, et al. Oral rizatriptan versus oral sumatriptan: a direct comparative study in the acute treatment of migraine. Headache 1998; 38: 748–55

    PubMed  Article  CAS  Google Scholar 

  30. Visser WH, Terwindt GM, Reines SA. Rizatriptan vs sumatriptan in the acute treatment of migraine: a placebo-controlled, dose-ranging study. Arch Neurol 1996 Nov; 53: 1132–7

    PubMed  Article  CAS  Google Scholar 

  31. Ahrens S, Farmer M, Williams D, et al. Efficacy and safety of rizatriptan wafer for the acute treatment of migraine. Cephalalgia 1999; 19: 525–30

    PubMed  Article  CAS  Google Scholar 

  32. Santanello NC, Polis AB, Hartmaier SL, et al. Improvement in migraine-specific quality of life in a clinical trial of rizatriptan. Cephalalgia 1997 Dec; 17: 867–72

    PubMed  Article  CAS  Google Scholar 

  33. Dasbach EJ, Gerth WC, Pigeon J, et al. Measuring the effect of acute migraine and its treatment on paid work and productivity loss in a randomized clinical trial of rizatriptan versus placebo [abstract]. Headache 1997 May; 37: 304–5

    Google Scholar 

  34. Lines C, Visser WH, Vandormael K, et al. Rizatriptan 5 mg versus sumatriptan 50 mg in the acute treatment of migraine [abstract]. Headache 1997 May; 37: 319–20

    Google Scholar 

  35. Silberstein S, Norman B, Jiang K, et al. Rizatriptan is effective in menstrual migraine [abstract]. Neurology 1999 Apr; 52 Suppl. 2: A208

    Google Scholar 

  36. Block GA, Goldstein J, Polis A, et al. Efficacy and safety of rizatriptan versus standard care during long-term treatment for migraine. Headache 1998; 38: 764–71

    PubMed  Article  CAS  Google Scholar 

  37. Heywood J, Zagami AS. Treating acute migraine attack: guidelines for general practitioners and emergency department doctors. Curr Ther 1997 Dec-Jan; 37: 33–7

    Google Scholar 

  38. Pryse-Phillips WEM, Dodick DW, Edmeads JG, et al. Guidelines for the diagnosis and management of migraine in clinical practice. Can Med Assoc J 1997 May 1; 156: 1273–87

    CAS  Google Scholar 

  39. Goa KL, Balfour JA. Management of acute migraine attacks: defining the role of sumatriptan. Dis Manage Health Outcomes 1997 Sep; 2: 141–55

    Article  Google Scholar 

  40. Gilkey SJ, Ramadan NM. Use of over-the-counter drugs in migraine: issues in self-medication. CNS Drugs 1996 Aug; 6: 83–9

    Article  Google Scholar 

  41. Glaxo Wellcome. Imigran prescribing information. ABPI compendium of data sheets and summaries of product characteristics, Datapharm Publications Limited, 1998–99

  42. Glaxo Wellcome. Naramig prescribing information. ABPI compendium of data sheets and summaries of product characteristics, Datapharm Publications Limited, 1998–99

  43. Zeneca Pharma. Zomig prescribing information. ABPI compendium of data sheets and summaries of product characteristics, Datapharm Publication Limited, 1998–99

  44. Glaxo Laboratories. Imitrex product information. PDR Generics. 53rd ed. Montevale NJ: Medical Economics, 1999

    Google Scholar 

  45. Zeneca Pharmaceuticals. Zomig product information. PDR Generics. 53rd ed. Montvale NJ: Medical Economics, 1999

    Google Scholar 

  46. Glaxo Wellcome Inc. Amerge product information. PDR Generics. 53rd ed. Montvale NJ: Medical Economics, 1999

    Google Scholar 

  47. Merck and Co. I. Maxalt, Maxalt-MLT product information. PDR Generics. 53rd ed. Montvale NJ: Medical Economics, 1999

    Google Scholar 

  48. Goldstein J. Current developments in 5-HT1Dreceptor agonists. Headache Q 1996; 7 Suppl. 2: 17–20

    Google Scholar 

  49. Bornhof MK, Legg N, Paz J. Comparison of rizatriptan 10mg versus naratriptan 2.5mg in migraine. Headache 1999; 39(5): 344

    Google Scholar 

  50. Diener HC, Pascual J, Vega P. Comparison of rizatriptan 10mg versus zolmitriptan 2.5mg in migraine. Headache 1999; 39(5): 351

    Google Scholar 

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Additional information

Various sections of the manuscript reviewed by: J. Edmeads, Sunnybrook Health Science Centre, University of Toronto, North York, Ontario, Canada; S. Evers, Department of Neurology, University of Münster, Münster, Germany; P. Goadsby, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England; J. Goldstein, San Francisco Headache Clinic, San Francisco, California, USA; M. Gross, The Royal and East Surrey Neurology Unit, Royal Surrey Country Hospital, Guildford, Surrey, England; W. Pryse-Phillips, Division of Neurology, Health Sciences Centre, Health Care Corporation of St. John’s, St. John’s, Newfoundland, Canada; P. Saxena, Department of Pharmacology, Erasmus University, Rotterdam, Netherlands; S. Silberstein, Department of Neurology, Jefferson Headache Center, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA.

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Dooley, M., Faulds, D. Rizatriptan. Drugs 58, 699–723 (1999). https://doi.org/10.2165/00003495-199958040-00013

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Keywords

  • Migraine
  • Adis International Limited
  • Sumatriptan
  • Migraine Attack
  • Zolmitriptan